Low Molecular Pectin Inhibited the Lipid Accumulation by Upregulation of METTL7B

Xiaojin Yang1, Yinghua Yuan2, Desheng Xie1

  • 1Department of Infectious Diseases, Shanghai Fifth People's Hospital, Fudan University, No. 128 Ruili Road, Shanghai, 200240, China.

Insights

Low-molecular-weight citrus pectin (LCP) reduces liver fat accumulation by increasing METTL7B, adipose triglyceride lipase (ATGL), and carnitine palmitoyltransferase-1 (CPT-1) levels. This suggests LCP may prevent nonalcoholic fatty liver disease progression.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Nutritional Science

Background:

  • Nonalcoholic fatty liver (NAFL) progression to nonalcoholic steatohepatitis is linked to lipid accumulation.
  • Targeting lipid accumulation is crucial for preventing NAFL progression.

Purpose of the Study:

  • To investigate the effect of low-molecular-weight citrus pectin (LCP) on lipid accumulation in liver cells.
  • To elucidate the underlying molecular mechanisms of LCP's action.

Main Methods:

  • An in vitro model using oleic acid (OA)-induced lipid deposition in HepG2 cells.
  • Oil Red O staining to quantify lipid accumulation.
  • RT-qPCR and RNA sequencing to analyze gene expression, including ATGL, CPT-1, and METTL7B.

Main Results:

  • LCP significantly reduced OA-induced lipid accumulation in HepG2 cells.
  • LCP treatment increased the expression of ATGL and CPT-1, key enzymes in lipid metabolism.
  • RNA sequencing identified METTL7B as a significantly upregulated gene, which, upon overexpression, also inhibited lipid accumulation and enhanced ATGL and CPT-1 levels.

Conclusions:

  • LCP inhibits lipid accumulation in liver cells, potentially by upregulating METTL7B.
  • The mechanism involves enhancing enzymes involved in triacylglycerol catabolism and fatty acid oxidation.
  • LCP shows promise as a therapeutic agent for managing fat accumulation in NAFL.

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